ROR1-AS1 knockdown inhibits growth and invasion and promotes apoptosis in NSCLC cells by suppression of the PI3K/Akt/mTOR pathway

The role of ROR1-AS1 in non-small-cell lung cancer (NSCLC) remains unclear. Therefore, we aimed to investigate the functional role of ROR1-AS1 in NSCLC and to explore the underlying mechanisms. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide assay was performed to detect cell proliferation. Transwell assay was performed to evaluate cell invasive ability. Cell apoptotic rates and caspase-3/7 activity were determined to evaluate apoptosis. The expression levels of PI3K/Akt/mTOR pathway-related proteins were measured using Western blot analysis. Results showed that ROR1-AS1 expression was upregulated in NSCLC samples. Knockdown of ROR1-AS1 inhibited the viability and invasive ability of NSCLC cells. Knockdown of ROR1-AS1 induced apoptotic rate and caspase-3/7 activity and suppressed xenograft NSCLC tumor growth. In addition, ROR1-AS1 knockdown inhibited the activation of the PI3K/Akt/mTOR pathway in NSCLC cells. However, treatment with 740Y-P prevented the effects of si-ROR1-AS1 on viability, invasive ability, and apoptosis of NSCLC cells. These findings implied that ROR1-AS1 played an oncogenic role in NSCLC via regulating the PI3K/Akt/mTOR pathway.

Automated summary

The study revealed that ROR1-AS1 is upregulated in NSCLC and knocking down ROR1-AS1 can inhibit the invasive ability and growth of NSCLC cells, inducing apoptosis by suppressing the activation of the PI3K/Akt/mTOR pathway.